About 40% of all insulin-dependent diabetic (IDDM) patients develop persistent albuminuria, a decline in their glomerular filtration rate and increased arterial blood pressure, collectively constituting the clinical syndrome of diabetic nephropathy. Diabetic nephropathy in the main cause of the increased morbidity and mortality in IDDM patients. The excess mortality of IDDM patients with nephropathy is 80 to 100 times that of the age-and sex-matched background population and is due to an enormous excess of cardiovascular mortality and end-stage renal disease (thousands of times the age-matched population). On average, death occurs eight years after start of persistent albuminuria. The cost for end-stage renal care in USA currently exceeds 0.8 billion dollars per year for diabetic nephropathy alone and is rapidly rising. Increased arterial pressure is an early and common occurrence in diabetic nephropathy. Fluid and sodium retention with normal concentrations of active renin, angiotensin I and II and aldosterone has been demonstrated in diabetic nephropathy. Systemic hypertension when transmitted to the glomerular capillary network results in glomerular capillary hypertension, which has also been shown in normotensive rats with streptozotocin diabetes. A link between glomerular hypertension and albuminuria and the development and progression of diabetic glomerulopathy has been suggested. Elevated blood pressure accelerates and effective blood pressure reduction with beta-blockers and/or ACE inhibitors delays the progression of nephropathy and reduces albuminuria. Apart from antihypertensive treatment, no other treatment modality has yet been proven to be effective in protection of kidney function in diabetic nephropathy. The introduction of effective antihypertensive treatment has increarsed the survival probability of the patients from 50 to 90% at eight years after the onset of albuminuria.